Neoplastic transformation of oral lichen planus :case report and review of the literatureBY : DR APARNA SRIVASTAVA.

chronic, immunological mucocutaneous disease with a widerange of clinical manifestations.

pre-malignant condition

a recall system has been recommended one to four times annuallyto facilitate the early diagnosis of malignant transformation.

Case report

60-year-old female

sharp and widespread pain in the oral cavity which had been present for approximately one

year and which worsened when in contact with food.

The most significant anamnestic findings were

cholecystectomy, 20 years previously, for gallstones;

chronic gastritis with hiatus hernia, under treatmentwithomeprazole and levosulpiride

hypothyroidism oral treatment with levothyroxine

asymptomatic hepatitis C virus (HCV) positive

non drinker, non smoker

mean corpuscular haemoglobin MCH)33.3 pg; erythrocyte sedimentation rate

(ESR) 27 mm/h

fibrinogen 403 mg/dl,

SGPT 52 IU/l,

Electrocardiogram (ECG) and chest X-ray were both negative

HISTOLOGICAL REPORTS

Fig. 1 Fig.2Fig. 1

Fig. 3 Fig. 4

Discussion

It is defined as a common chronic immunological

mucocutaneousdisorder that varies in appearnce from

keratotic to erythematous and ulcerative Wilson

1896

Lichen planus is relatively common

disorder of the stratified

squamous epithelia skullyand El-kom1985

Eisen D 2005 defined oral

lichen planus as a relatively

common chronic inflammatory

disorder affecting the

statifiedsquamous epithelia

A common disorder in which auto-

cytotoxic T lymphocytes trigger

apoptosis of epithelial cells

leading to chronic inflammation. Oral LP (OLP) can be a source of severe

morbidity and has a small potential to be malignant. Crispian

Scully 2007

Common mucocutaneous disease with varying clinical presentation

Also known as Lichen Rubber Planus

First described clinically :- 1869 – Wilson

Erasmus Wilson (1869)-Mixed non Scrapable Red and white lesion in themouth-Can occur individually or with skin lesions.

*Lichen in Greek – tree moss *Planus in Latin – flat.

Epidemiology

• 1% of general population is affected

• 0.14-0.8% worldwide

• 2/3rd of cases occur in middle age

• No racial predilection reported although some authors claims a predilection in blacks

• Increased in the month of Jun-July & Dec-Jan

• Male: Female - 1:1• 20% females with oral lesions have genital involvement

• 2/3rd of the cases are symptomatic• 40%- of patients have both Oral & Cutaneous lesions

• 35%- of patients have Cutaneous lesions only• 25%- of the cases presents with mucosal lesions only

Buccal mucosa often bilaterally

Tongue

Lip

Gingiva

Patate

Floor of mouth

Co

mm

on

si

tes

"5 P's“

Pruritic

planar

Purple

Polygonal

papules

Louis frederic wickham described the

presence of fine white or grey lines or dots

seen on the top of the pruritic rash on the skin

in lichen planus . These striae are popularly

referred to as “WICKHAMS STRIAE or

HONITON LACE” Text book of oral

medicine and radiology –ongole first edition

ETIOLOGY

Etiology is unknown.

Immune System has a primary role

in the development

of this disease.

Genetic background

Dental materials-metallic &

non metallic restoration

Drugs & chemicals

Infectious agents

AutoimmunityChronic liver

disease Immunodefici

encies

subepithelial band–formed infiltrate dominated by T lymphocytes,macrophages and the degeneration of basal cells known as liquefaction degeneration .

expression of the cell-mediated immune system being involved in the pathogenesis of OLP

T-lymphocyte cytotoxicity directed against antigens

expressed by the basal cell layer.

Pathogenesis of lichen planus; TCR-T cell receptor, MHC-Major histocompatibility receptor, TNF-Tumor necrosis factor, MMP-Matrix metalloproteinases

photomicrography

FIRST DESCRIBE

D BY DUBRENIL

L 1906 later

revised by Shklar in

1972

RETICULAR FORM

• white lines or striae.

• The striae may form a network but can also

show annular (circular) patterns.

• The striae often display a peripheral

erythematous zone, which reflects the

subepithelial inflammation.

• all regions of the oral mucosa, most

frequently this form is observed bilaterally in

the buccal mucosa and rarely on the mucosal

side of the lips.

• sometimes at the vermilion border.

PAPULAR FORMpresent in the initial phase of the disease.

It is clinically characterized by small white dots, which in most occasions intermingle with the reticular form.

Sometimes the papular elements merge with striae as part of the natural course.

Plaque-type

shows a homogeneous well-demarcated white plaque often.

Plaque-type lesions may clinically be very similar to homogeneous oral leukoplakias.

The difference between these two mucosal disorders is the simultaneous presence of reticular or papularstructures in the case of plaque-like OLP.

This form is most often encountered in smokers andollowing cessation

plaque may disappear and convert into the reticular type of OLP.

Some scientific reports lend support to the premise that plaque-like OLP is overrepresented among OLP lesions transforming into oral squamous cell carcinomas

Erythematous lichen planus

Erosive type

Bullous typeVesciculobullous presentation combined with reticular or erosive pattern

Rare form characterized by large vesicles or bullae (4mm to 2cm)

Lesions usually develop within an erythematus base, rupture immediately leaving painful ulcers

Usually have peripheral radiating striae and seen on posterior part of buccal mucosa

type Incidence percent

Reticular 94

Atrophic 44

Plaque like 36

Papular 11

Atrophic 9

Erosive 1

Modified World Health Organization diagnostic criteria of OLPPresence of bilateral, more or less symmetrical lesions

Presence of a lacelike network of slightly raised gray- white lines(reticular pattern)

Erosive, atrophic, bullous and plaque-type lesions are accepted only as a subtype in the presence of reticular lesion else where in the oral mucosa

In all other lesions that resemble OLP but do not complete the aforemented criteria, the term “clinically compatible with” should be used.

IncidenceMalignant potentialThe most important complication of OLP is the development of oral squamous cell carcinoma.

Frequency of malignant transformation varies greatly, between 0.4% to over 5%, over periods of observation from 0.5 to over 20 years (van der Meijet al, 1999).

Significantly increased risk of oral cancer appears to be independent of the clinical type of OLP and therapy administered (Gandolfo et al, 2004)

Considerable controversy regarding themalignant transformation of OLP. Despite the fact thatmore than 25 follow-up studies have focused on this topic, as recently reviewed by Barnard et al (Barnardet al, 1993)

scrupulous attention is necessary

concomitant skin invasion

of lichen,

HCV infection

HBV infection

autoimmune diseases.

Malignant transformation observed

3 months after lichen planus with lichenoid dysplasia

3 months after lichenoid dysplasia and ulcerated infiltrating cancer G1-G2

suggests the need for histopathological observations at more frequent intervals (at least every 3months) from the time of the first diagnosis

Incidence :

Erosive type Ulcerative type Atrophic type Plaque type

Investigations

• Incisional biopsy• Immunoflourescent studies-Fluorescent

dyes like FITC

• Immunoglobulin assay

• PAS staining

Treatment planning

Differential diagnosis

1. Lychenoid reaction

2. Graft verses host response

3. Leukoplakia

4. Frinctional keratosis

REASON FOR CHOOSING THIS ARTICLE

1. Kilpi A, Rich AM, Reade PC, Konttinen YT. Studies of the inflammatory process and malignant potential of oral mucosal lichen planus. Aust Dent J 1996;41:87-90.

2. Ognjenovic M, Karelovic D, Cindro VV, Tadin I. Oral lichen planus and HLA A. Coll Antropol1998;22:89-92

3.\Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and Maxillofacial Pathology. 2nd ed. Saunders: Elsevier; 2005. p. 89.

4. BURKET’S ORAL MEDICINE 11TH EDITION BY GREENBERG,GLICK,SHIP CBS PUBLISHERS AND DISTRIBUTERS

5. DIAGNOSTIC OF ORAL MEDICINE, B K Venkatraman 1st Edition,Willams and Wilkins publishers

6. Roy K, Bagg J. Hepatitis C virus and oral disease: a critical Review. Oral Dis 1999;5:270-7.

7. Rajendran R, Sivapathasundaram B. Shafer’s Textbook of Oral Pathology.6th ed.Elsevier.Dehli; 2009: p.48-54 Radiology.